ArticleBMC gastroenterology2025
Expression of kinetochore component NDC80 promotes esophageal squamous cell carcinoma cells proliferation and migration.
Article in BMC gastroenterology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNDC80, a crucial component of the kinetochore, plays a pivotal role in regulating cell mitosis. Recent studies reported that NDC80 regulates the proliferation of cancer cells and may be related to poor prognosis in cancer. However, the biological function and mechanism of NDC80 in esophageal squamous cell carcinoma (ESCC) have not yet been elucidated. In this study, we analyzed the expression and mutation of NDC80 in ESCC tissue and assessed its impact on ESCC cells in vitro.
methodsA total of 52 ESCC tissues samples were collected and NDC80 gene status was analyzed by whole exome sequence. shRNA was used to knockdown NDC80 expression in two ESCC cell lines TE1 and ECA109 by targeting silence NDC80 gene. Cellular proliferation, apoptosis, migration, and invasion were examined.
resultsCopy number variants (CNVs) of NDC80 were detected in 40.4% (21/52) cancer tissues. Genes with local CNVs values greater than 0.3 were classified as "gain". 23.1% (12/52) of cases showed CNVs gain and 58.3% (7/12) of which with genotype of AAB. Compared with patients of other NDC80 CNVs status, CNVs gain patients had relatively shorter overall survival, however with no statistic difference (19.9 ± 0.8 months vs. 30.9 ± 5.1 months, p = 0.124). Single nucleotide polymorphism mutation of NDC80 was detected in only 5.8% (3/52) cancer tissues including two previous reported mutation rs2271754 and rs6506019, and one novel SNP of C/A-T/G in 2,577,492, GRCh38.p13 intron variant in one case. The knockdown of NDC80 in vitro assays significantly suppressed cellular proliferation and induced increased apoptosis in both TE1 and ECA109 cells. Furthermore, the migration and invasion ability of both TE1 and ECA109 cells were also attenuated upon knockdown of NDC80.
conclusionCNVs were identified as the predominant genetic variation of NDC80 gene in ESCC patients. In vitro assays suggested that NDC80 was not only involved into proliferation and apoptosis but also migration and invasion of ESCC cells.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.